Histopathological study on the pathogenesis of intratarsal keratinous cyst

Abstract

Purpose : Intratarsal Keratinous Cyst (IKC) is a recently described entity that is frequently misdiagnosed clinically as chalazia and mislabelled in literature as “intratarsal epidermal inclusion cysts.” It is important to accurately diagnose IKC and distinguish them from epidermal inclusion cysts because IKC requires a complete surgical excision and can exhibit multiple recurrences following curettage. The pathogenesis of IKC’s developmental stages has not been fully studied. As well, there remain contradicting reports on which histochemical or immunohistological stains are the most valuable in diagnosing IKC. We performed a retrospective case series to further elucidate the pathogenesis of IKC and to determine the diagnostically optimal panel of stains for diagnosis.

Methods : A study group of eight IKC specimens were obtained from the registry of the Ottawa Hospital. Epidermal inclusion cysts of the eyelid were used as controls. We compared the immunohistochemical profile of IKC and epidermal inclusion cyst by staining each specimen with hematoxylin and eosin (H-E), periodic acid-Schiff stain (PAS), Masson trichrome, cytokeratin 5 (CK5), cytokeratin 17 (CK17), carcinoembryonic antigen (CEA), and epithelial membrane antigen (EMA). The immunoreactivity data were then analyzed using chi-square test (p<0.05 is significant).

Results : Histopathologically, IKC was embedded in the tarsus lined by stratified squamous epithelium with an inner undulating cuticle filled with a compact keratinous-appearing material. IKC was shown to develop progressively from dilated meibomian ducts to formation of complete cysts with the use of histochemical and immunohistological markers. The most valuable markers to diagnose IKC were found to be CK17, CEA, and EMA (p <0.05 with each). CK17 stained the cyst and meibomian acini. EMA stained all of the above in addition to conjunctiva. CEA stained the cyst and conjunctiva. CK5 stained the cyst, meibomian acini, conjunctiva, and epidermis, and thus is not helpful in differentiating from epidermal structures.

Conclusions : Our study further elucidates the pathogenesis of IKC through its origin from the meibomian duct rather than being derived as an epidermal cyst, as well as clarifies much of the controversy concerning which immunostains to use for the diagnosis of IKC. These findings allow a better understanding of this new entity for more appropriate diagnosis and treatment to reduce future complications.

This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.